Ritchlin C
Clinical Immunology & Rheumatology Unit, University of Rochester Medical Center, Rochester, New York 14642, USA.
Arthritis Res. 2000;2(5):356-60. doi: 10.1186/ar112. Epub 2000 Jun 23.
There is mounting evidence indicating that the synovial fibroblast is a direct effector of tissue injury and matrix remodeling in inflammatory synovitis. Through the elaboration of effector signals including cytokines and chemokines, mesenchymal cells stimulate or suppress inflammation via autocrine and paracrine mechanisms. Synovial fibroblasts are the principal cells mediating joint destruction through secretion of metalloproteinases, and recent evidence suggests that they may also promote bone resorption by stimulating osteoclastogenesis. Moreover, they may play an integral role in the initial phases of synovitis by releasing chemokines that recruit leukocytes to the joint, and cytokines that trigger angiogenesis. Studies focusing on synoviocyte-leukocyte interactions mediated via the cytokine network and the role of cell-cell contact in driving synoviocyte activation will help define the complex interplay that leads to the initiation and perpetuation of synovial inflammation.
越来越多的证据表明，滑膜成纤维细胞是炎症性滑膜炎中组织损伤和基质重塑的直接效应器。通过分泌包括细胞因子和趋化因子在内的效应信号，间充质细胞通过自分泌和旁分泌机制刺激或抑制炎症。滑膜成纤维细胞是通过分泌金属蛋白酶介导关节破坏的主要细胞，最近的证据表明它们也可能通过刺激破骨细胞生成来促进骨吸收。此外，它们可能通过释放趋化因子招募白细胞至关节以及释放触发血管生成的细胞因子，在滑膜炎的初始阶段发挥不可或缺的作用。专注于通过细胞因子网络介导的滑膜细胞 - 白细胞相互作用以及细胞 - 细胞接触在驱动滑膜细胞活化中的作用的研究，将有助于确定导致滑膜炎症起始和持续的复杂相互作用。
